Melatonin inhibits the proliferation of breast cancer cells induced by bisphenol A via targeting estrogen receptor-related pathways.

Abstract

BackgroundBackground: Bisphenol A (BPA) is an estrogen‐like chemical widely contained in daily supplies. There is evidence that environmental exposure to BPA could contribute to the development of hormone‐related cancers. As is reported in numerous studies, melatonin, an endogenous hormone secreted by the pineal gland, could markedly inhibit estrogen‐induced proliferation of breast cancer (BC) cells. In this study, we intended to reveal the effects of melatonin on BPA‐induced proliferation of estrogen receptor‐positive BC cells.MethodsMethods: We used methyl thiazolyl tetrazolium, luciferase reporter gene and western blotting assays to testify the effect of melatonin on BPA‐mediated proliferation of MCF‐7 and T47D cells.ResultsMethyl thiazolyl tetrazolium and colony formation assays showed that melatonin could significantly abolish BPA‐elevated cell proliferation. Meanwhile, BPA‐upregulated phosphorylation of ERK and AKT was decreased by melatonin treatment. Mechanistically, we found that BPA was capable of upregulating the protein levels of steroid receptor coactivators (SRC‐1, SRC‐3), as well as promoting the estrogen response element activity. However, the addition of melatonin could remarkably block the elevation of steroid receptor coactivators expression and estrogen response element activity triggered by BPA.ConclusionConclusions: Therefore, these results demonstrated that melatonin could abrogate BPA‐induced proliferation of BC cells. Therapeutically, melatonin could be regarded as a potential medication for BPA‐associated BC.